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An experimental study on resuscitation of tissue dysoxia

组织缺氧复苏的实验研究

基本信息

批准号：
16591809
负责人：
AOKI Katsunori
金额：
$ 2.18万
依托单位：
Hamamatsu University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

The purpose of this study was to evaluate tissue dysoxia in an experimental model of hemorrhagic shock and endotoxin shock. Ten rabbits (Japan White Rabbits, BW 3kg) were assigned to 2 groups. Group A (n=5) was resuscitated by blood transfusion and Group B (n=5) by isotonic crystalloid solution. The value of ileum serosal oxygen partial pressure was about 30 mmHg lower by the method of Pd-porphyrin phsophorescense than by the method of the oxygen electrodes. The reason why the two methods provided different data was that Pd-porphyrin phsophorescense measured the tissue oxygen pressure in the deeper layer of ileum than the oxygen electrode. The value of ileum serosal oxygen partial pressure decreased in hemorrhagic shock and showed lower than the value of venous oxygen partial pressure. This gap of oxygen partial pressure between tissue and vein was apparently seen in the group resuscitated by crystalloid solution. This shunt effect seen in the hemorrhagic shock was significantly prevented with hyperoxia. On the other hand, a decrease in ileal serosal oxygen partial pressure and persistent negative oxygen gap between tissue and vein was seen in endotoxin shock model induced by LPS(Escherichia coli-055:B5, mg/kg) in 10 animals. We conclude that tissue dysoxia may form at an early stage in hemorrhagic shock and endotoxin shock and shunting of the microcirculation may be an important contributing factor to development of multiple organ failure. To evaluate the severity of the shunting effect, new technologies aimed at the microcirculation will need to be developed about analysis of heterogenous distribution of oxygen in tissue.

本研究的目的是评估失血性休克和内毒素休克实验模型中的组织缺氧。将10只家兔（日本白色家兔，BW 3 kg）分为2组。A组（n=5）采用输血复苏，B组（n=5）采用等渗晶体液复苏。用钯-卟啉磷电极法测定的回肠血清氧分压比氧电极法低30 mmHg左右。两种方法提供的数据不同的原因是钯卟啉磷光法比氧电极法测量的是回肠深层的组织氧分压。失血性休克时回肠浆膜氧分压降低，并低于静脉氧分压。在晶体液复苏组中，组织和静脉之间的氧分压差明显。这种在失血性休克中观察到的分流效应可通过高氧显著预防。另一方面，在10只动物的LPS（Escherichia coli-055：B5，mg/kg）诱导的内毒素休克模型中，观察到回肠浆膜氧分压降低和组织与静脉之间的持续负氧隙。我们的结论是，组织缺氧可能形成于早期阶段的失血性休克和内毒素休克和微循环的分流可能是一个重要的促成因素，多器官功能衰竭的发展。为了评估分流效应的严重程度，需要开发针对微循环的新技术来分析组织中氧的不均匀分布。